| Project/Area Number |
21790114
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Drug development chemistry
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| Research Institution | Kumamoto University |
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Principal Investigator |
KAWAHARA Kohichi Kumamoto University, 大学院・生命科学研究部, 助教 (10347015)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2009: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | アルツハイマー病 / ミクログリア / CD36 / レチノイド / インターロイキン-4 / 2型ミクログリア / インターロイキン4 / レチノイン酸受容体 / レチノイドX受容体 / モルヒネアナローグ / アミロイドβ |
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| Research Abstract |
As a new strategy for treatment of Alzheimer's disease (AD), we aimed to induce the antiinflammatory activity we have in a living body. In particular, we tried to develop the strategy for which the neuroprotective anti-inflammatory type of microglia (type 2 MG) is utilized aggressively and searched the new medicine seeds which achieves this. When we administered an intracerebral microinjection of a mixture of IL-4 and IL-13 into one hemisphere of 4.5 mo old APP23 mice, CD36-positive MG was induced at 2 day, and A β accumulation was reduced at 7 day post injection. The cytokine-induced CD36 expression was observed in arginase I-positive and Ym1-positive cells, which indicates that CD36-positive MG are M2-like cells (Kawahara et al., submitted). We found that oral administration of retinoic acid receptor agonist Am80, which increased IL-4 production in T-cell system, decreased brain Aβ42 peptide in APP23 mice (Kawahara et al., Biol. Pharm. Bull., 2009). This study may encourage development of new anti-inflammatory strategies for treatment of AD.
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